MINOCA and ACS mimics

• Alternative causes of a trop rise +/- abnormal ECG
  • • PE
      • • Negative T waves in leads III and V1 occur in 1% of patients with ACS compared with 88% of patients with Acute PE
        • Consider echo for right heart strain to differentiate at bedside
    • Arrhythmias
      • • Can cause troponin to rise up to 100 or so
    • SAH
    • MINOCA
      • • Incl Myocarditis and Takotsubos (see below)
    • Aortic dissection
      • • Consider if abrupt, tearing pain, radiation to back, risk factors
    • Various acute/chronic illnesses (Type 2 MI)
      • • Sepsis, hypovolaemia / shock, anaemia, hypoxia, AKI/CKD, COPD, HF
    • Autoimmune myositis
      • • The elevated trop T is from skeletal muscle. Check trop I – should be normal as this is specific for cardiac muscle damage
• Mimics of ACS-like pain
  • • Pericarditis
    • Aortic dissection
    • PE
    • GI – reflux, biliary tract, perforated peptic ulcer, pancreatitis
• Mimics of STEMI (ie chest pain, ST elevation, positive troponin)
  • • Myocarditis
    • Takotsubo’s cardiomyopathy
    • Previous LV aneurysm (causes ST elevation. Trop might be chronically a bit elevated. Chest pain would occur for another reason)
    • Brugada syndrome – Downsloping ST segment elevation

---

MINOCA (MI with non-obstructive coronary arteries)

• An umbrella term used post angiography, that includes various pathologies
  • • Coronary
      • • Coronary embolism, coronary microvascular dysfunction, coronary spasm, coronary thrombosis, myocardial bridging, plaque rupture, SCAD
    • Non-coronary cardiac
      • • Cardiac trauma, cardiomyopathy, cardiotoxins, myocarditis, strenuous exercise, Takotsubos cardiomyopathy, transplant rejection
    • Non-cardiac
      • • ARDS, hypersensitivity reactions, ESRF, inflammation, PE, sepsis, CVA
• Probably occurs in around 8% of patients with ACS undergoing angiography
• Can present with chest pain and elevated troponin
• Be wary of high risk NSTEMI with severe pain and normal ECG
• Investigation
  • • Cause of MINOCA might be diagnosed on angiogram (esp if also testing for microvascular dysfunction or vasoreactivity – ‘functional coronary angiogram’)
    • Cardiac MRI often useful (can diagnose 87% of cases, and should be done as soon as possible)
    • Consider CTPA

---

Specific causes of MINOCA

• Stress (Takotsubo) cardiomyopathy
  • • 27% of MINOCA, 1-2% of ACS.
    • ST elevated in anterior leads with normal coronaries
    • MRI shows mid to apical wall motion abnormality with oedema and no scar
    • Apical ballooning on echo (Takotsubo is Japanese for ‘lobster pot’)
    • Often females with a history of severe stress
    • Sometimes background drug use or DM
    • LAD affected usually
    • 96% recover in 40 days
    • Treat with standard heart failure meds until LV function recovers (and sometimes give betablockers long term). Only give aspirin if evidence of atherosclerosis. No prospective RCT evidence here.
• Spontaneous coronary artery dissection (SCAD)
  • • Can also be associated with emotional stress or occurs during intense exertion
    • Often occurs peripartum, during the menopause, or in those on hormonal treatment
    • Sometimes associated connective tissue disease
    • Typically affects young women without risk factors
    • Angiogram can be reported as normal – consider repeat
    • Same pharmacological treatment given as type 1 MI (although more data needed)
    • PCI is not generally advised and has a high rate of complications (perhaps >30%). Consider PCI or CABG only if ongoing ischaemia, a large area of myocardium in jeopardy or reduced antegrade flow
    • Treatment is medical
• Coronary artery spasm
  • • Associated with cocaine use
• Myocarditis – 37% of MINOCA
• Cardiomyopathies
• Type 1 myocardial infarction!
  • • Up to 10% of MIs have normal coronaries on angio
    • Can be due to
      • • Angiogram operator missing the problem. People have a different number of septal branches of the LAD, so lesions can be missed
        • An embolism (and rarely due to a fibroelastoma on a heart valve which can embolise)
        • Plaque rupture and recanalization
• Type 2 MI
  • • Due to:
      • • Oxygen supply/demand imbalance (with or without atherosclerosis)
        • Eg sustained tachyarrhythmia or bradyarrthymia, severe HTN/LVH, respiratory failure, severe anaemia, shock, coronary spasm or embolism
• Coronary microvascular dysfunction
• Non atherosclerotic coronary dissection
  • • Similar or higher mortality than STEMI or NSTEMI
    • Causes include arrythmias, heart failure, myocarditis, Takotsubos, aortic dissection, PE, AKI, neurological event, severe AS, critical illness / sepsis. Cardiac contusion/procedure, thyroid disease. Infiltrative disease, toxins, extreme endurance / rhabdo
    • Aspirin is still sometimes given, esp if diagnosis uncertain, but certainly not if patient is anaemic as high risk of GI bleed